Chronic exposure to nicotine alters endothelium-dependent arteriolar dilatation: Effect of superoxide dismutase

William G. Mayhan, Glenda M. Sharpe

Research output: Contribution to journalArticle

69 Citations (Scopus)

Abstract

The first goal of this study was to determine whether chronic injection of nicotine alters endothelium-dependent arteriolar dilatation. We measured the diameter of cheek pouch resistance arterioles (~50 μm in diameter) in response to endothelium-dependent (acetylcholine and ADP) and -independent (nitroglycerin) agonists in control hamsters and hamsters treated with nicotine (2 μg·kg-1·day-1 for 2-3 wk). In control hamsters, acetylcholine (0.1 and 1.0 μM) dilated arterioles by 13 ± 2 and 31 ± 3%, respectively, and ADP (1.0 and 10 μM) dilated arterioles by 18 ± 1 and 30 ± 1%, respectively. In contrast, acetylcholine (0.1 and 1.0 μM) dilated arterieles by only 5 ± 2 and 12 ± 3%, respectively, and ADP (1.0 and 10 μM) dilated arterioles by only 7 ± 2 and 13 ± 3%, respectively, in animals treated with nicotine (P < 0.05 vs. response in control hamsters). Nitroglycerin produced similar dose-related dilatation of cheek pouch arterioles in control and nicotine-treated hamsters. Our second goal was to examine a possible mechanism for impaired endothelium-dependent arteriolar dilatation during chronic treatment with nicotine. We found that superfusion of the cheek pouch microcirculation with superoxide dismutase (150 U/ml) restored impaired endothelium-dependent, but did not alter endothelium- independent, arteriolar dilatation in hamsters treated with nicotine. Superfusion with superoxide dismutase did not alter endothelium-dependent or -independent arteriolar dilatation in control hamsters. We suggest that chronic exposure to nicotine produces selective impairment of endothelium- dependent arteriolar dilatation via a mechanism related to the synthesis/release of oxygen-derived free radicals.

Original languageEnglish (US)
Pages (from-to)1126-1134
Number of pages9
JournalJournal of Applied Physiology
Volume86
Issue number4
DOIs
StatePublished - Apr 1999

Fingerprint

Nicotine
Cricetinae
Superoxide Dismutase
Endothelium
Dilatation
Arterioles
Cheek
Adenosine Diphosphate
Acetylcholine
Nitroglycerin
Microcirculation
Free Radicals
Oxygen
Injections

Keywords

  • Acetylcholine
  • Adenosine 5'-diphosphate
  • Arterioles
  • Cheek pouch
  • Endothelium-derived relaxing factor
  • Hamsters
  • N(G)-monomethyl-L-arginine
  • Nitric oxide
  • Nitroglycerin
  • Oxygen radicals

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Chronic exposure to nicotine alters endothelium-dependent arteriolar dilatation : Effect of superoxide dismutase. / Mayhan, William G.; Sharpe, Glenda M.

In: Journal of Applied Physiology, Vol. 86, No. 4, 04.1999, p. 1126-1134.

Research output: Contribution to journalArticle

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abstract = "The first goal of this study was to determine whether chronic injection of nicotine alters endothelium-dependent arteriolar dilatation. We measured the diameter of cheek pouch resistance arterioles (~50 μm in diameter) in response to endothelium-dependent (acetylcholine and ADP) and -independent (nitroglycerin) agonists in control hamsters and hamsters treated with nicotine (2 μg·kg-1·day-1 for 2-3 wk). In control hamsters, acetylcholine (0.1 and 1.0 μM) dilated arterioles by 13 ± 2 and 31 ± 3{\%}, respectively, and ADP (1.0 and 10 μM) dilated arterioles by 18 ± 1 and 30 ± 1{\%}, respectively. In contrast, acetylcholine (0.1 and 1.0 μM) dilated arterieles by only 5 ± 2 and 12 ± 3{\%}, respectively, and ADP (1.0 and 10 μM) dilated arterioles by only 7 ± 2 and 13 ± 3{\%}, respectively, in animals treated with nicotine (P < 0.05 vs. response in control hamsters). Nitroglycerin produced similar dose-related dilatation of cheek pouch arterioles in control and nicotine-treated hamsters. Our second goal was to examine a possible mechanism for impaired endothelium-dependent arteriolar dilatation during chronic treatment with nicotine. We found that superfusion of the cheek pouch microcirculation with superoxide dismutase (150 U/ml) restored impaired endothelium-dependent, but did not alter endothelium- independent, arteriolar dilatation in hamsters treated with nicotine. Superfusion with superoxide dismutase did not alter endothelium-dependent or -independent arteriolar dilatation in control hamsters. We suggest that chronic exposure to nicotine produces selective impairment of endothelium- dependent arteriolar dilatation via a mechanism related to the synthesis/release of oxygen-derived free radicals.",
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N2 - The first goal of this study was to determine whether chronic injection of nicotine alters endothelium-dependent arteriolar dilatation. We measured the diameter of cheek pouch resistance arterioles (~50 μm in diameter) in response to endothelium-dependent (acetylcholine and ADP) and -independent (nitroglycerin) agonists in control hamsters and hamsters treated with nicotine (2 μg·kg-1·day-1 for 2-3 wk). In control hamsters, acetylcholine (0.1 and 1.0 μM) dilated arterioles by 13 ± 2 and 31 ± 3%, respectively, and ADP (1.0 and 10 μM) dilated arterioles by 18 ± 1 and 30 ± 1%, respectively. In contrast, acetylcholine (0.1 and 1.0 μM) dilated arterieles by only 5 ± 2 and 12 ± 3%, respectively, and ADP (1.0 and 10 μM) dilated arterioles by only 7 ± 2 and 13 ± 3%, respectively, in animals treated with nicotine (P < 0.05 vs. response in control hamsters). Nitroglycerin produced similar dose-related dilatation of cheek pouch arterioles in control and nicotine-treated hamsters. Our second goal was to examine a possible mechanism for impaired endothelium-dependent arteriolar dilatation during chronic treatment with nicotine. We found that superfusion of the cheek pouch microcirculation with superoxide dismutase (150 U/ml) restored impaired endothelium-dependent, but did not alter endothelium- independent, arteriolar dilatation in hamsters treated with nicotine. Superfusion with superoxide dismutase did not alter endothelium-dependent or -independent arteriolar dilatation in control hamsters. We suggest that chronic exposure to nicotine produces selective impairment of endothelium- dependent arteriolar dilatation via a mechanism related to the synthesis/release of oxygen-derived free radicals.

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